Eicke Latz

Summary

Affiliation: University of Massachusetts Medical School
Country: USA

Publications

  1. ncbi request reprint Cutting edge: Immune stimulation by neisserial porins is toll-like receptor 2 and MyD88 dependent
    Paola Massari
    Department of Medicine, Division of Infectious Diseases, Boston University School of Medicine, Boston, MA 02118, USA
    J Immunol 168:1533-7. 2002
  2. ncbi request reprint Lipopolysaccharide rapidly traffics to and from the Golgi apparatus with the toll-like receptor 4-MD-2-CD14 complex in a process that is distinct from the initiation of signal transduction
    Eicke Latz
    University of Massachusetts Medical School, Division of Infectious Diseases, Worcester 01605, USA
    J Biol Chem 277:47834-43. 2002
  3. ncbi request reprint Haemophilus influenzae type b-outer membrane protein complex glycoconjugate vaccine induces cytokine production by engaging human toll-like receptor 2 (TLR2) and requires the presence of TLR2 for optimal immunogenicity
    Eicke Latz
    Department of Medicine, University of Massachusetts Medical Center, Worcester, MA 01605, USA
    J Immunol 172:2431-8. 2004
  4. ncbi request reprint Mechanisms of TLR9 activation
    Eicke Latz
    Division of Infectious Diseases, University of Massachusetts Medical School, 364 Plantation Street, LRB 370M, Worcester, MA 01605, USA
    J Endotoxin Res 10:406-12. 2004
  5. ncbi request reprint Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE
    Jane Tian
    Inflammation and Autoimmune Group, Research Department, MedImmune, Gaithersburg, Maryland 20878, USA
    Nat Immunol 8:487-96. 2007
  6. pmc NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
    Peter Duewell
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nature 464:1357-61. 2010
  7. pmc Influence of genetic variations in TLR4 and TIRAP/Mal on the course of sepsis and pneumonia and cytokine release: an observational study in three cohorts
    Oliver Kumpf
    Department of Anesthesiology, Intensive Care Medicine and Pain Management, HANSE Klinikum Stralsund, Grosse Parower Strasse 47 53, Stralsund 18435, Germany
    Crit Care 14:R103. 2010
  8. ncbi request reprint The LPS receptor generates inflammatory signals from the cell surface
    Eicke Latz
    Division of Infectious Diseases, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    J Endotoxin Res 9:375-80. 2003
  9. ncbi request reprint Ligand-induced conformational changes allosterically activate Toll-like receptor 9
    Eicke Latz
    Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nat Immunol 8:772-9. 2007
  10. pmc The inflammasomes: mechanisms of activation and function
    Eicke Latz
    University of Massachusetts Medical School, Department of Infectious Diseases and Immunology, 364 Plantation St, Worcester, MA 01605, USA
    Curr Opin Immunol 22:28-33. 2010

Detail Information

Publications53

  1. ncbi request reprint Cutting edge: Immune stimulation by neisserial porins is toll-like receptor 2 and MyD88 dependent
    Paola Massari
    Department of Medicine, Division of Infectious Diseases, Boston University School of Medicine, Boston, MA 02118, USA
    J Immunol 168:1533-7. 2002
    ..This is the first demonstration of known vaccine adjuvant to stimulate immune cells via TLR2...
  2. ncbi request reprint Lipopolysaccharide rapidly traffics to and from the Golgi apparatus with the toll-like receptor 4-MD-2-CD14 complex in a process that is distinct from the initiation of signal transduction
    Eicke Latz
    University of Massachusetts Medical School, Division of Infectious Diseases, Worcester 01605, USA
    J Biol Chem 277:47834-43. 2002
    ..Golgi-associated TLR4 expression was disrupted by brefeldin A, yet LPS signaling was preserved. We conclude that LPS signaling may be initiated by surface aggregation of TLR4 and is not dependent upon LPS trafficking to the Golgi...
  3. ncbi request reprint Haemophilus influenzae type b-outer membrane protein complex glycoconjugate vaccine induces cytokine production by engaging human toll-like receptor 2 (TLR2) and requires the presence of TLR2 for optimal immunogenicity
    Eicke Latz
    Department of Medicine, University of Massachusetts Medical Center, Worcester, MA 01605, USA
    J Immunol 172:2431-8. 2004
    ..TLR2 engagement by an adjuvant or carrier protein may be a useful strategy for augmentation of the anti-PS Ab response induced by glycoconjugate vaccines...
  4. ncbi request reprint Mechanisms of TLR9 activation
    Eicke Latz
    Division of Infectious Diseases, University of Massachusetts Medical School, 364 Plantation Street, LRB 370M, Worcester, MA 01605, USA
    J Endotoxin Res 10:406-12. 2004
    ..In stimulated cells, TLR9 translocated to CpG-DNA or microbial DNA containing structures in the endosome, where TLR9 binds to DNA and initiates signaling...
  5. ncbi request reprint Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE
    Jane Tian
    Inflammation and Autoimmune Group, Research Department, MedImmune, Gaithersburg, Maryland 20878, USA
    Nat Immunol 8:487-96. 2007
    ..Our data demonstrate a mechanism by which HMGB1 and RAGE activate plasmacytoid dendritic cells and B cells in response to DNA and contribute to autoimmune pathogenesis...
  6. pmc NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
    Peter Duewell
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nature 464:1357-61. 2010
    ..These findings provide new insights into the pathogenesis of atherosclerosis and indicate new potential molecular targets for the therapy of this disease...
  7. pmc Influence of genetic variations in TLR4 and TIRAP/Mal on the course of sepsis and pneumonia and cytokine release: an observational study in three cohorts
    Oliver Kumpf
    Department of Anesthesiology, Intensive Care Medicine and Pain Management, HANSE Klinikum Stralsund, Grosse Parower Strasse 47 53, Stralsund 18435, Germany
    Crit Care 14:R103. 2010
    ....
  8. ncbi request reprint The LPS receptor generates inflammatory signals from the cell surface
    Eicke Latz
    Division of Infectious Diseases, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    J Endotoxin Res 9:375-80. 2003
    ..Thus, LPS signaling commences after LPS recognition by surface-expressed TLR4 independent of LPS trafficking to the Golgi...
  9. ncbi request reprint Ligand-induced conformational changes allosterically activate Toll-like receptor 9
    Eicke Latz
    Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nat Immunol 8:772-9. 2007
    ..Our results indicate that the formation of TLR9 dimers is not sufficient for its activation but instead that TLR9 activation is regulated by conformational changes induced by DNA containing CpG...
  10. pmc The inflammasomes: mechanisms of activation and function
    Eicke Latz
    University of Massachusetts Medical School, Department of Infectious Diseases and Immunology, 364 Plantation St, Worcester, MA 01605, USA
    Curr Opin Immunol 22:28-33. 2010
    ..Recent work proposes that NLRP3 is activated indirectly by host factors that are generated in response to NLRP3 triggers...
  11. ncbi request reprint The interferon regulatory factor, IRF5, is a central mediator of toll-like receptor 7 signaling
    Annett Schoenemeyer
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    J Biol Chem 280:17005-12. 2005
    ..IRF5 and IRF7, therefore, emerge from these studies as critical mediators of TLR7 signaling...
  12. pmc Cutting edge: NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression
    Franz G Bauernfeind
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Immunol 183:787-91. 2009
    ..Signals provided by NF-kappaB activators are necessary but not sufficient for NLRP3 activation, and a second stimulus such as ATP or crystal-induced damage is required for NLRP3 activation...
  13. ncbi request reprint TLR9 signals after translocating from the ER to CpG DNA in the lysosome
    Eicke Latz
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Lazare Research Building 308, 364 Plantation Street, Worcester, MA 01605, USA
    Nat Immunol 5:190-8. 2004
    ..Our data indicate a previously unknown mechanism of cellular activation involving the recruitment of TLR9 from the ER to sites of CpG DNA uptake, where signal transduction is initiated...
  14. ncbi request reprint Lysines 128 and 132 enable lipopolysaccharide binding to MD-2, leading to Toll-like receptor-4 aggregation and signal transduction
    Alberto Visintin
    Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    J Biol Chem 278:48313-20. 2003
    ..These findings help clarify the earliest events of TLR4 triggering by LPS and identify MD-2 as an attractive target for pharmacological intervention in endotoxin-mediated diseases...
  15. pmc LPS-TLR4 signaling to IRF-3/7 and NF-kappaB involves the toll adapters TRAM and TRIF
    Katherine A Fitzgerald
    Division of Infectious Disease and Immunology, Department of Medicine, The University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Exp Med 198:1043-55. 2003
    ..These studies suggest that TRIF and TRAM both function in LPS-TLR4 signaling to regulate the MyD88-independent pathway during the innate immune response to LPS...
  16. pmc The AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses
    Vijay A K Rathinam
    Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA
    Nat Immunol 11:395-402. 2010
    ..Collectively, our observations demonstrate the importance of AIM2 in the sensing of both bacterial and viral pathogens and in triggering innate immunity...
  17. pmc The myristoylation of TRIF-related adaptor molecule is essential for Toll-like receptor 4 signal transduction
    Daniel C Rowe
    Division of Infectious Disease and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Proc Natl Acad Sci U S A 103:6299-304. 2006
    ....
  18. pmc AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC
    Veit Hornung
    Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nature 458:514-8. 2009
    ..Collectively, these observations identify AIM2 as a new receptor for cytoplasmic DNA, which forms an inflammasome with the ligand and ASC to activate caspase-1...
  19. pmc Dual engagement of the NLRP3 and AIM2 inflammasomes by plasmodium-derived hemozoin and DNA during malaria
    Parisa Kalantari
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Cell Rep 6:196-210. 2014
    ..Finally, infected erythrocytes activated both the NLRP3 and AIM2 inflammasomes. These observations suggest that Hz and DNA work together to induce systemic inflammation during malaria. ..
  20. pmc TLR-independent type I interferon induction in response to an extracellular bacterial pathogen via intracellular recognition of its DNA
    Marie Charrel-Dennis
    Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Cell Host Microbe 4:543-54. 2008
    ..Thus, activation of IFN-alpha/-beta production during infection with GBS, commonly considered an extracellular pathogen, appears to result from the interaction of GBS DNA with a putative intracellular DNA sensor or receptor...
  21. pmc Importance of extra- and intracellular domains of TLR1 and TLR2 in NFkappa B signaling
    Frantisek Sandor
    Department of Medicine, University of Massachusetts Medical Center, Worcester, MA 01605 2324, USA
    J Cell Biol 162:1099-110. 2003
    ..The domains from each receptor did not need to be contained within a single contiguous protein. Chimeric TLR analysis further defined the toll/IL-1R domains as the area of crucial intracellular TLR1-TLR2 interaction...
  22. pmc Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization
    Veit Hornung
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nat Immunol 9:847-56. 2008
    ..Our results indicate that the NALP3 inflammasome senses lysosomal damage as an endogenous 'danger' signal...
  23. pmc The NALP3 inflammasome is involved in the innate immune response to amyloid-beta
    Annett Halle
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Nat Immunol 9:857-65. 2008
    ..Our findings suggest that activation of the NALP3 inflammasome is important for inflammation and tissue damage in Alzheimer's disease...
  24. pmc CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation
    Frederick J Sheedy
    Department of Medicine, Marc and Ruti Bell Program for Vascular Biology and Disease, The Leon H Charney Division of Cardiology, New York University School of Medicine, New York, New York, USA
    Nat Immunol 14:812-20. 2013
    ..Collectively, our findings highlight the importance of CD36 in the accrual and nucleation of NLRP3 ligands from within the macrophage and position CD36 as a central regulator of inflammasome activation in sterile inflammation. ..
  25. pmc Inflammasomes: too big to miss
    Andrea Stutz
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA
    J Clin Invest 119:3502-11. 2009
    ..We discuss the current knowledge of the mechanisms leading to the activation of cytoplasmic, multimolecular protein complexes, termed "inflammasomes," which regulate the activity of caspase-1 and the maturation and release of IL-1beta...
  26. ncbi request reprint Flavivirus activation of plasmacytoid dendritic cells delineates key elements of TLR7 signaling beyond endosomal recognition
    Jennifer P Wang
    Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Immunol 177:7114-21. 2006
    ..A greater understanding of viral RNA-TLR7 activity relationships will promote rational approaches to interventional and vaccine strategies for important human viral pathogens...
  27. ncbi request reprint Pharmacological inhibition of endotoxin responses is achieved by targeting the TLR4 coreceptor, MD-2
    Alberto Visintin
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Immunol 175:6465-72. 2005
    ..The ability to inhibit the effects of LPS as a result of the binding of TLR4-Fc or E5564 to MD-2 highlights MD-2 as the logical target for drug therapies designed to pharmacologically intervene against endotoxin-induced disease...
  28. pmc RAGE is a nucleic acid receptor that promotes inflammatory responses to DNA
    Cherilyn M Sirois
    Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605
    J Exp Med 210:2447-63. 2013
    ..Furthermore, mice deficient in RAGE were unable to mount a typical inflammatory response to DNA in the lung, indicating that RAGE is important for the detection of nucleic acids in vivo. ..
  29. doi request reprint Overexpression of membrane-bound fas ligand (CD95L) exacerbates autoimmune disease and renal pathology in pristane-induced lupus
    Lukas Bossaller
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Immunol 191:2104-14. 2013
    ..These results demonstrate that FasL promotes inflammation in TMPD-induced autoimmunity, and its cleavage limits FasL proinflammatory activity. ..
  30. pmc Cutting edge: FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner
    Lukas Bossaller
    Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Immunol 189:5508-12. 2012
    ..Hence, Fas controls a novel noncanonical IL-1β activation pathway in myeloid cells, which could play an essential role in inflammatory processes, tumor surveillance, and control of infectious diseases...
  31. pmc Malaria hemozoin is immunologically inert but radically enhances innate responses by presenting malaria DNA to Toll-like receptor 9
    Peggy Parroche
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Proc Natl Acad Sci U S A 104:1919-24. 2007
    ..However, its activity depends on being bound to HZ, which we propose amplifies the biological responses to malaria DNA by targeting it to a TLR9(+) intracellular compartment...
  32. doi request reprint The sterile inflammatory response
    Kenneth L Rock
    Department of Pathology, University of Massachusetts Medical School, Worcester, 01655, USA
    Annu Rev Immunol 28:321-42. 2010
    ..Here we review established and emerging data about these responses...
  33. ncbi request reprint IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway
    Katherine A Fitzgerald
    Division of Infectious Disease and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Nat Immunol 4:491-6. 2003
    ..Thus, IKKepsilon and TBK1 have a pivotal role in coordinating the activation of IRF3 and NF-kappaB in the innate immune response...
  34. pmc Natural loss-of-function mutation of myeloid differentiation protein 88 disrupts its ability to form Myddosomes
    Kamalpreet Nagpal
    Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    J Biol Chem 286:11875-82. 2011
    ..The MyD88 S34Y loss-of-function mutant demonstrates how proper cellular localization of MyD88 to the Myddosome is a feature required for MyD88 function...
  35. doi request reprint Toll-like receptor interactions imaged by FRET microscopy and GFP fragment reconstitution
    Gabor Horvath
    Eicke Latz Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Methods Mol Biol 517:33-54. 2009
    ..These techniques permit the dynamic visualization of early signaling events in living cells and can be utilized in pharmacological or genetic screens...
  36. pmc Receptor "cross talk" in innate immunity
    Eicke Latz
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    J Clin Invest 112:1136-7. 2003
    ..The report reveals yet another way in which the primordial innate immune system is remarkably complex...
  37. pmc Human cytomegalovirus activates inflammatory cytokine responses via CD14 and Toll-like receptor 2
    Teresa Compton
    McArdle Laboratory for Cancer Research, University of Wisconsin Madison Medical School, Madison, Wisconsin 53706, USA
    J Virol 77:4588-96. 2003
    ..Since many of the pathological processes associated with CMV disease are facilitated or directly mediated by inflammatory cytokines, identification of the host membrane detection machinery may ultimately lead to improved therapeutics...
  38. ncbi request reprint Cell distributions and functions of Toll-like receptor 4 studied by fluorescent gene constructs
    Terje Espevik
    Norwegian University of Science and Technology, Trondheim, Norway
    Scand J Infect Dis 35:660-4. 2003
    ..Furthermore, LPS stimulation recruited the adapter molecule, MyD88, to the inside of the plasma membrane. Thus, LPS signaling commences on the plasma membrane and is independent of trafficking to the Golgi...
  39. ncbi request reprint Involvement of toll-like receptor (TLR) 2 and TLR4 in cell activation by mannuronic acid polymers
    Trude H Flo
    Institute of Cancer Research and Molecular Biology and the Institute of Biotechnology, Norwegian University of Science and Technology, 7489 Trondheim, Norway
    J Biol Chem 277:35489-95. 2002
    ..Taken together the results suggest that both TLR2 and TLR4 are involved in cell activation by poly-M and that TLR4 may be required in primary murine macrophages...
  40. ncbi request reprint The antifungal drug amphotericin B promotes inflammatory cytokine release by a Toll-like receptor- and CD14-dependent mechanism
    Keya Sau
    Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 278:37561-8. 2003
    ..Our results provide a putative molecular basis for inflammatory responses elicited by amphotericin B and suggest strategies to eliminate the acute toxicity of this drug...
  41. ncbi request reprint A novel host-parasite lipid cross-talk. Schistosomal lyso-phosphatidylserine activates toll-like receptor 2 and affects immune polarization
    Desiree van der Kleij
    Department of Parasitology, Leiden University Medical Center, The Netherlands
    J Biol Chem 277:48122-9. 2002
    ..Taken together, these findings provide evidence for a novel host-parasite interaction that may be central to long term survival of the parasite and limited host pathology with implications beyond parasitology...
  42. ncbi request reprint Cryptococcus neoformans glycoantigens are captured by multiple lectin receptors and presented by dendritic cells
    Michael K Mansour
    Department of Microbiology and Immunology Training Program, Boston University School of Medicine, Boston, MA 02118, USA
    J Immunol 176:3053-61. 2006
    ..These data suggest that DC provide the crucial link between innate and adaptive immune responses to C. neoformans via a process that is dependent upon the efficient uptake of mannoprotein by mannose receptors...
  43. ncbi request reprint Poxvirus protein N1L targets the I-kappaB kinase complex, inhibits signaling to NF-kappaB by the tumor necrosis factor superfamily of receptors, and inhibits NF-kappaB and IRF3 signaling by toll-like receptors
    Gary DiPerna
    Viral Immune Evasion Group, Department of Biochemistry, Trinity College, Dublin 2, Ireland
    J Biol Chem 279:36570-8. 2004
    ..Furthermore, N1L inhibited IRF3 signaling, which is also regulated by TBK1. These studies define a role for N1L as an immunomodulator of innate immunity by targeting components of NF-kappaB and IRF3 signaling pathways...
  44. ncbi request reprint Recruitment and endo-lysosomal activation of TLR9 in dendritic cells infected with Trypanosoma cruzi
    Daniella C Bartholomeu
    Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
    J Immunol 181:1333-44. 2008
    ..cruzi genome are likely to be main parasite targets and probably become available to TLR9 when parasites are destroyed in the lysosome-fused vacuoles during parasite invasion/uptake by phagocytes...
  45. pmc Human lupus autoantibody-DNA complexes activate DCs through cooperation of CD32 and TLR9
    Terry K Means
    Center for Immunology and Inflammatory Diseases and Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    J Clin Invest 115:407-17. 2005
    ....
  46. doi request reprint The DNA sugar backbone 2' deoxyribose determines toll-like receptor 9 activation
    Tobias Haas
    Institut fur Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universitat Munchen, Trogerstrasse 30, 81675 Munchen, Germany
    Immunity 28:315-23. 2008
    ....
  47. ncbi request reprint HMGB1 signals through toll-like receptor (TLR) 4 and TLR2
    Man Yu
    Laboratories of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    Shock 26:174-9. 2006
    ..Taken together, our data suggest that there is a differential usage of TLR2 and TLR4 in HMGB1 signaling in primary cells and in established cell lines, adding complexity to studies of HMGB1 signaling which was not previously expected...
  48. pmc Endocytic pathways regulate Toll-like receptor 4 signaling and link innate and adaptive immunity
    Harald Husebye
    Institute of Cancer Research and Molecular Medicine, The Norwegian University of Science and Technology, Trondheim, Norway
    EMBO J 25:683-92. 2006
    ..Our results show that endosomal trafficking of the LPS receptor complex is essential for signal termination and LPS-associated antigen presentation, thus controlling both innate and adaptive immunity through TLR4...
  49. ncbi request reprint TLR9 and the recognition of self and non-self nucleic acids
    Marc S Lamphier
    Eisai Research Institute, Andover, Massachusetts 01810, USA
    Ann N Y Acad Sci 1082:31-43. 2006
    ..We therefore propose that there is an additional recognition step by which TLR9 senses differences in the structures of bound DNA...
  50. pmc Comparative toll-like receptor 4-mediated innate host defense to Bordetella infection
    Paul B Mann
    Pathobiology Graduate Program, Immunology Research Laboratories, Department of Veterinary Science, The Pennsylvania State University, University Park, PA 16802, USA
    Infect Immun 73:8144-52. 2005
    ..Thus, it appears that in adapting to infect humans, B. pertussis and B. parapertussis independently modified their LPS to reduce TLR4-mediated responses, which may compensate for slower growth rates and facilitate host colonization...
  51. doi request reprint Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis
    Masataka Asagiri
    Department of Cell Signaling, Graduate School, Tokyo Medical and Dental University, Tokyo 113 8549, Japan
    Science 319:624-7. 2008
    ..These results suggest that cathepsin K plays an important role in the immune system and may serve as a valid therapeutic target in autoimmune diseases...
  52. pmc SPTLC1 binds ABCA1 to negatively regulate trafficking and cholesterol efflux activity of the transporter
    Norimasa Tamehiro
    Lipid Metabolism Unit and Center for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, Massachusetts 02114, USA
    Biochemistry 47:6138-47. 2008
    ..In composite, these results indicate that the physical interaction of ABCA1 and SPTLC1 results in reduction of ABCA1 activity and that inhibition of this interaction produces enhanced cholesterol efflux...
  53. ncbi request reprint Pentoxifyllin attenuates the systemic inflammatory response induced during isolated limb perfusion with recombinant human tumor necrosis factor-alpha and melphalan
    Peter Hohenberger
    Division of Surgery and Surgical Oncology, Robert Rössle Hospital and Tumor Institute, Max Delbruck Center for Molecular Medicine, Berlin, Germany
    Ann Surg Oncol 10:562-8. 2003
    ..Pentoxifyllin (PTX) produced a beneficial effect on cytokine response and survival in animal experiments of septic shock, and we were interested to explore its effect during TNF-ILP in humans...

Research Grants3

  1. Inflammasome activation by cholesterol crystals
    Eicke Latz; Fiscal Year: 2010
    ..Understanding the molecular mechanisms of cholesterol crystal recognition can lead to novel molecular targets for therapies that prevent inflammation in atherosclerotic lesions, which can improve or prevent atherosclerotic disease. ..
  2. Inflammasome activation by cholesterol crystals
    Eicke Latz; Fiscal Year: 2009
    ..Understanding the molecular mechanisms of cholesterol crystal recognition can lead to novel molecular targets for therapies that prevent inflammation in atherosclerotic lesions, which can improve or prevent atherosclerotic disease. ..
  3. Role of PISA; a PYHIN Family Member in Intracellular DNA Recognition
    Eicke Latz; Fiscal Year: 2009
    ..Elucidation of molecular details of PISA activation could lead to novel strategies of pharmacological interference for diseases based on intracellular DNA recognition. ..